These studies involve the interaction of humoral antibodies with lymphocytes to affect tumor cell destruction. Using antibodies with specificity for virally determined antigens, antibody-dependent cell-mediated cytotoxicity (ADCC) has been demonstrated with thymocytes as effector cells. Both IgM and IgG induced cell-mediated cytotoxicity. There was no requirement for C5 for the induction of ADCC by either IgM or IgG. Also, C5 is not required for in vivo tumor regression of M-MuSV tumors. The cortisone resistant subpopulation of medullary thymocytes was the most efficient effector cell against antibody-sensitized target cells. The receptors responsible for binding of thymus processed lymphocytes to antibody-sensitized target cells and subsequent induction of ADCC include receptors for the Fc portion of IgM and Fc portion of IgG on T cells. Also, a receptor for the third component of complement has been found on a small subpopulation of thymocytes following cortisone involution. The divalent cation requirements for binding of IgM, IgG and C3 to the surface of mouse lymphocytes is being studied. Magnesium but not calcium supports the binding of IgM and C3 to spleen cells and calcium can interfere with IgM Fc receptor binding. Calcium potentiates the binding of IgG. These data suggest that one might be able to specifically activate tumor patients' own T cells against their tumor using passive administration of the appropriate class or subclass of antibody.